Heteromeric KCNQ5/Q3 channels were stably expressed in Chinese Hamster ovary cells and characterized using the whole cell voltage-clamp technique. KCNQ5/Q3 channels were activated by the novel anticonvulsant, retigabine (EC50 1.4 μM) by a mechanism that involved drug-induced, leftward shifts in the voltage-dependence of channel activation (-31.8 mV by 30 μM retigabine). KCNQ5/Q3 channels were inhibited by linopirdine (IC50 7.7 μM) and barium (IC50 0.46 mM), at concentrations similar to those required to inhibit native M-currents. These findings identify KCNQ5/Q3 channels as a molecular target for retigabine and raise the possibility that activation of KCNQ5/Q3 channels may be responsible for some of the anti-convulsant activity of this agent. Furthermore, the sensitivity of KCNQ5/Q3 channels to linopirdine supports the possibility that potassium channels comprised of KCNQ5 and KCNQ3 may make a contribution to native M-currents.
CITATION STYLE
Wickenden, A. D., Zou, A., Wagoner, P. K., & Jegla, T. (2001). Characterization of KCNQ5/Q3 potassium channels expressed in mammalian cells. British Journal of Pharmacology, 132(2), 381–384. https://doi.org/10.1038/sj.bjp.0703861
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